In exchange for a nutrient-rich home, gut microbiota help the host digest food and stimulate host immunity. Pickard et al. report that the host actively feeds its gut commensals during systemic infections to maintain this mutually beneficial relationship. Pathogen-derived molecules activate Toll-like receptors (TLRs) to trigger innate immune responses to infection. Injecting any of several TLR agonists into mice rapidly induced fucosylation of surface molecules that persisted for several days throughout the small intestine. This did not occur in mice lacking the TLR adaptor protein MyD88 or the fucosyltransferase Fut2. TLR signaling in dendritic cells induced the release of interleukin-23 (IL-23), which stimulated innate lymphoid cells to release IL-22, ultimately inducing Fut2 expression in epithelial cells of the small intestine. Loss of appetite (anorexia) and weight loss often occurs with infection, and intestinal microbiota can survive this reduction in dietary nutrients by consuming host-derived sugars. Injecting lipopolysaccharide (LPS) into Fut2+/-, Fut2-/-, or germ-free mice induced symptoms of infection, including anorexia and transient weight loss. However, Fut2-/- mice and mice lacking intestinal microbiota took longer to recover weight lost due to LPS-induced anorexia than did normally colonized Fut2+/- mice. LPS also triggered a Fut2-dependent increase in the amount of fucosylated proteins present in the intestinal lumen, including an increase in the abundance of fucosylated mucins and digestive enzymes. Bacterial fucosidases cleaved these secreted glycoproteins, releasing fucose that was consumed by gut microbiota. Expression of microbial virulence genes was increased in Fut2-/- mice compared to Fut2+/- mice, suggesting that fucosylation also suppressed virulence of resident gut microbiota. When Fut2+/- and Fut-+/- mice infected with the intestinal pathogen Citrobacter rodentium were challenged with LPS, the mice exhibited similar numbers of C. rodentium in the colon. However, the Fut2-/- mice lost more weight and had more C. rodentium–induced colonic hyperplasia. The authors propose that the fucose provided by the host may contribute to recovery from infection by supporting gut commensals, suppressing virulence of opportunistic pathogens, and altering pathogen virulence to allow the host to tolerate the pathogen. Rakoff-Nahoum and Comstock discuss the role of intestinal fucosylation in both infection and steady-state contexts.